Cardiplegin

Cardiplegin Uses, Dosage, Side Effects, Food Interaction and all others data.

Magnesium chloride salts are highly soluble in water and the hydrated form of magnesium chloride can be extracted from brine or sea water.

Magnesium is important as a cofactor in many enzymatic reactions in the body involving protein synthesis and carbohydrate metabolism (at least 300 enzymatic reactions require magnesium). Actions on lipoprotein lipase have been found to be important in reducing serum cholesterol and on sodium/potassium ATPase in promoting polarization (eg, neuromuscular functioning).

Potassium chloride is a major cation of the intracellular fluid. It plays an active role in the conduction of nerve impulses in the heart, brain and skeletal muscle; contraction of cardiac skeletal and smooth muscles; maintenance of normal renal function, acid-base balance, carbohydrate metabolism and gastric secretion.

The potassium ion is in the principle intracellular cation of most body tissues. Potassium ions participate in a number of essential physiological processes including the maintenance of intracellular tonicity, the transmission of nerve impulses, the contraction of cardiac, skeletal and smooth muscle, and the maintenance of normal renal function. The intracellular concentration of potassium is approximately 150 to 160 mEq per liter. The normal adult plasma concentration is 3.5 to 5 mEq per liter. An active ion transport system maintains this gradient across the plasma membrane. Potassium is a normal dietary constituent and under steady-state conditions the amount of potassium absorbed from the gastrointestinal tract is equal to the amount excreted in the urine. The usual dietary intake of potassium is 50 to 100 mEq per day. Potassium depletion will occur whenever the rate of potassium loss through renal excretion and/or loss from the gastrointestinal tract exceeds the rate of potassium intake. Such depletion usually develops as a consequence of therapy with diuretics, primarily or secondary hyperaldosteronism, diabetic ketoacidosis, or inadequate replacement of potassium in patients on prolonged parenteral nutrition. Depletion can develop rapidly with severe diarrhea, especially if associated with vomiting. Potassium depletion due to these causes is usually accompanied by concomitant loss of chloride and is manifested by hypokalemia and metabolic alkalosis. Potassium depletion may produce weakness, fatigue, disturbances of cardiac rhythm (primarily ectopic beats), prominent U-waves in the electrocardiogram, and, in advanced cases, flaccid paralysis and/or impaired ability to concentrate urine. If potassium depletion associated with metabolic alkalosis cannot be managed by correcting the fundamental cause of the deficiency, e.g., where the patient requires long-term diuretic therapy, supplemental potassium in the form of high potassium food or potassium chloride may be able to restore normal potassium levels. In rare circumstances (e.g., patients with renal tubular acidosis) potassium depletion may be associated with metabolic acidosis and hyperchloremia. In such patients, potassium replacement should be accomplished with potassium salts other than the chloride, such as potassium bicarbonate, potassium citrate, potassium acetate, or potassium gluconate.

A local anesthetic of the ester type that has a slow onset and a short duration of action. It is mainly used for infiltration anesthesia, peripheral nerve block, and spinal block. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1016). Procaine has also been investigated as an oral entry inhibitor in treatment-experienced HIV patients .

Procaine is an anesthetic agent indicated for production of local or regional anesthesia, particularly for oral surgery. Procaine (like cocaine) has the advantage of constricting blood vessels which reduces bleeding, unlike other local anesthetics like lidocaine. Procaine is an ester anesthetic. It is metabolized in the plasma by the enzyme pseudocholinesterase through hydrolysis into para-aminobenzoic acid (PABA), which is then excreted by the kidneys into the urine.

Cardiplegin
Uses
Dosage
Side Effect
Precautions
Interactions
Uses during Pregnancy
Uses during Breastfeeding
Accute Overdose
Food Interaction
Half Life
Volume of Distribution
Clearance
Interaction With other Medicine
Contradiction
Storage

Trade Name	Cardiplegin
Generic	Magnesium Chloride + Potassium Chloride + Procaine
Type	Injection
Therapeutic Class
Manufacturer	Troikaa Pharmaceuticals Ltd
Available Country	India
Last Updated:	September 19, 2023 at 7:00 am

Uses

Magnesium chloride is an ionic compound and source of magnesium used for electrolyte replenishment and conditions associated with magnesium deficiencies.

Magnesium chloride is used in several medical and topical (skin related) applications. Magnesium chloride usp, anhydrous uses as electrolyte replenisher, pharmaceutic necessity for hemodialysis and peritoneal dialysis fluids.

Potassium chloride is used for drug induced hypokalemia, liver cirrhosis, nausea, vomiting, cholera, diarrhoea, muscular weakness, paralysis, cardiac and congestive heart failure, diabetic ketoacidosis, ulcerative colitis, weakness, anorexia, drowsiness, Cushing's syndrome, pyloric stenosis, low blood pressure etc.

Procaine is a local anesthetic used for anesthesia, peripheral nerve block, and spinal nerve block.

Used as a local anesthetic primarily in oral surgery

Cardiplegin is also used to associated treatment for these conditions: Electrolyte imbalance, Magnesium Deficiency, Mild Metabolic acidosis, Automated peritoneal dialysis, Continuous Renal Replacement Therapy, Continuous ambulatory peritoneal dialysis therapy, Fluid replacement therapy, Hemodialysis Treatment, Irrigation therapy, Organ Preservation, Parenteral rehydration therapy, Peritoneal dialysis therapy, Total parenteral nutrition therapy, Urine alkalinization therapy, Fluid and electrolyte maintenance therapyDehydration, Dry Mouth, Hypokalemia, Hypotonic Dehydration, Hypovolaemia, Isotonic Dehydration, Markedly Reduced Food Intake, Metabolic Acidosis, Hypodermoclysis, Mild Metabolic acidosis, Mild, moderate Metabolic Acidosis, Ocular edema, Acid-Base Balance, Bowel preparation therapy, Electrolyte replacement, Fluid replacement therapy, Hemodialysis Treatment, Hemofiltration, Parenteral Nutrition, Parenteral rehydration therapy, Plasma Volume Replacement, Urine alkalinization therapy, Fluid and electrolyte maintenance therapyOtalgia

How Cardiplegin works

Mechanism of action of magnesium chloride studied in 10 adult volunteers. Results suggested magnesium ion in duodenum is relatively weak stimulus to pancreas and gall bladder. It is weak stimulant to cholecystokinin release and inhibits net jejunal water absorption. The oral administration of a single 800 mg dose of magnesium chloride in healthy volunteers resulted in a diminished rate of intraluminal lipid and protein digestion. The most pronounced effect of magnesium chloride, however, was a decreased gastric emptying rate of both test meals. After correction for gastric emptying, no differences were noted in intraluminal lipid or protein digestion. Therefore, the lower lipid levels noted after magnesium supplementation are unlikely to be the result of altered lipid assimilation. Magnesium chloride slows gastric emptying but does not influence lipid digestion.

Supplemental potassium in the form of high potassium food or potassium chloride may be able to restore normal potassium levels.

Procaine acts mainly by inhibiting sodium influx through voltage gated sodium channels in the neuronal cell membrane of peripheral nerves. When the influx of sodium is interrupted, an action potential cannot arise and signal conduction is thus inhibited. The receptor site is thought to be located at the cytoplasmic (inner) portion of the sodium channel. Procaine has also been shown to bind or antagonize the function of N-methyl-D-aspartate (NMDA) receptors as well as nicotinic acetylcholine receptors and the serotonin receptor-ion channel complex.

Dosage

Cardiplegin dosage

Oral:Dosage must be adjusted to the individual needs of each patient.

Adults: In severe deficiencies 3-6 tablets or 4-8 teaspoonful or 25-50 mmol per day orally in divided doses for some days with fruit juice, sweet or plain water.
Children: ½-1 teaspoonful twice daily or 1-3 mmol/kg body weight a day in several divided doses.

Patient should take Potassium chloride with meals.

Intravenous:

Severe acute hypokalaemia:

Adult: If serum potassium level >2.5 mEq/L, give at a rate not exceeding 10 mEq/hr in a concentration of up to 40 mEq/L. Max dose: 200 mEq/24 hr. If serum potassium level <2 mEq/L, may infuse at a rate of up to 40 mEq/hr. Continuous cardiac monitoring is essential. Max dose: 400 mEq/24 hr.

75 mg KCl equivalent to 1 mmol K+

Side Effects

GI ulceration (sometimes with haemorrhage and perforation or with late formation of strictures) following the use of enteric-coated K chloride preparation; hyperkalaemia. Oral: Nausea, vomiting, diarrhoea and abdominal cramps. IV: Pain or phloebitis; cardiac toxicity.

Toxicity

Mouse LD50 775mg/kg (intraperitoneal) Mouse LD50 : 7600mg/kg (oral) Rat LD 50 : 8100mg/kg (oral) Rat LD50 176mg/kg (intravenous) Severe toxicity occurs most often after intravenous infusions. It can also occur after chronic excessive oral doses, often in patients with renal insufficiency. Early manifestations are lethargy, hyporeflexia, followed by weakness, paralysis, hypotension, ECG changes (prolonged PR and QRS intervals), CNS depression, seizures, and respiratory depression. In overdose, magnesium impairs neuromuscular transmission, manifested as weakness and hyporeflexia.

The administration of oral potassium salts to persons with normal excretory mechanisms for potassium rarely causes serious hyperkalemia. However, if excretory mechanisms are impaired, of if potassium is administered too rapidly intravenously, potentially fatal hyperkalemia can result. It is important to recognize that hyperkalemia is usually asymptomatic and may be manifested only by an increased serum potassium concentration (6.5-8.0 mEq/L) and characteristic electrocardiographic changes (peaking of T-waves, loss of P-wave, depression of S-T segment, and prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9-12 mEq/L).

Precaution

Renal or adrenocortical insufficiency; cardiac disease; acute dehydration; extensive tissue destruction. Pregnancy. Ensure adequate urine output; monitor plasma-potassium and other electrolyte concentrations. Discontinue treatment if severe nausea, vomiting or abdominal distress develops. Accumulation of potassium may occur in renal impairment.

Interaction

Potassium-sparing diuretics, ACE inhibitors, ciclosporin and potassium-containing drugs. Antimuscarinics delay gastric emptying time consequently increasing risk of GI adverse effects esp of solid oral dosage forms.

Volume of Distribution

Bone (50% to 60%); extracellular fluid (1% to 2%)

Elimination Route

Oral: Inversely proportional to amount ingested; 40% to 60% under controlled dietary conditions; 15% to 36% at higher doses

Potassium is a normal dietary constituent and under steady-state conditions the amount of potassium absorbed from the gastrointestinal tract is equal to the amount excreted in the urine.

Half Life

Elimination half-life has been reported to be 27.7 hours following an overdose of 400 mEq magnesium in an adult.

7.7 minutes

Clearance

Maximum magnesium clearance is directly proportional to creatinine clearance.

Elimination Route

Magnesium is excreted in urine. Unabsorbed magnesium is excreted in feces

Potassium is a normal dietary constituent and, under steady-state conditions, the amount of potassium absorbed from the gastrointestinal tract is equal to the amount excreted in the urine. Potassium depletion will occur whenever the rate of potassium loss through renal excretion and/or loss from the gastrointestinal tract exceeds the rate of potassium intake.

With normal kidney function, the drug is excreted rapidly by tubular excretion.

Pregnancy & Breastfeeding use

Category C: Either studies in animals have revealed adverse effects on the foetus (teratogenic or embryocidal or other) and there are no controlled studies in women or studies in women and animals are not available. Drugs should be given only if the potential benefit justifies the potential risk to the foetus.